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JCI online early table of contents: Feb. 7, 2008
Date:2/7/2008

ce they trafficked normally unless the mice were administered an inflammatory stimulus that induced a tissue to express the molecule (known as an antigen) that the T cells recognized. Under these conditions, the T cells from mice expressing an inactive form of PI3K p110-delta failed to migrate and to accumulate in the antigenic tissue, meaning that an immune response was not mounted. Consistent with this, normal T cells treated with a drug that inhibits PI3K p110-delta did not migrate to antigenic tissues activated by an inflammatory stimulus. The authors therefore suggested that drugs inhibiting PI3K p110-delta might be useful in preventing unwanted T cell accumulation in tissues, such as occurs in some autoimmune diseases and inflammatory disorders.

TITLE: T cell receptorinduced phosphoinositide-3-kinase p110-delta activity is required for T cell localization to antigenic tissue in mice

AUTHOR CONTACT:
Federica Marelli-Berg
Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Phone: 44-0-2083831704; Fax: 44-0-2083832788; E-mail: f.marelli@imperial.ac.uk.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33267


GASTROENTEROLOGY: The soluble factor IL-10 has guts

Although it is known that the soluble factor IL-10 has an important role in preventing inflammation in the intestine of mice, the function of IL-10 in the human intestine is not well understood. By studying explant cultures of human colonic mucosa (the lining of the large intestine), Anne Jarry and colleague,s at INSERM U539, France, have now shown that IL-10 prevents a damaging inflammatory response being induced by bacteria living naturally in the human colon.

IL-10 was found to be constitutively expressed and secreted by human colonic mucosa. Depletion of IL-10 in explan
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press_releases@the-jci.org
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Journal of Clinical Investigation
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